It has been appreciated for over 30 years that visual experience during an early postnatal critical period of development produces permanent modifications of the connectivity, physiology and function of the visual cortex. Besides the obvious relevance of this neural plasticity to the development of visual capabilities in humans and animals, it seems likely that similar processes form the basis for some forms of learning and memory in the adult brain. Considerable progress has been made in identifying the specific changes in visual cortex that result from rearing the animals in different environments, but the detailed mechanisms that underlie these modifications have remained elusive. Recently, however, advances in understanding the receptor mechanisms that mediate synaptic excitation and inhibition in the visual cortex during development have provided an exciting new opportunity to investigate the mechanisms of experience-dependent brain modification. The long-term goal of this project is to elucidate these molecular mechanisms of experience-dependent cortical plasticity. It is hypothesized that naturally occurring synaptic enhancements employ the mechanisms that underlie long-term synaptic potentiation (LTP), a type of plasticity that can be elicited in cortical synapses by tetanic electrical stimulation. To examine this hypothesis, a preparation has been introduced in which LTP can be elicited in the geniculo-cortical projection in vivo. Our first aim is to determine if experience dependent synaptic enhancement and LTP utilize a common saturable expression mechanism by (1) probing LTP saturation limits after experience-dependent synaptic enhancement, and (2) by saturating the expression mechanism for LTP and determining if this occludes or prevents the effects of experience. These experiments will address the question of whether the expression mechanisms of LTP are necessary for aspects of experience-dependent cortical plasticity, and vice versa. Our second aim is to determine if the mechanisms of LTP are sufficient to cause the same changes as visual experience in visual cortical (1) glutamate receptors (phosphorylation and distribution), and (2) population synaptic currents (evoked with visual stimulation or electrical stimulation of the LGN). These experiments promise to establish that LTP and naturally occurring synaptic plasticity utilize common mechanisms.